Baicalin promotes the survival of flaps by downregulating the JAK2-STAT3 signaling pathway.

BACKGROUND

Skin flaps are commonly employed in wound reconstruction and plastic surgery, yet frequently develop distal necrosis post-transplantation. Baicalin, a principal bioactive compound derived from the traditional Chinese medicinal herb Scutellaria baicalensis Georgi, has not been systematically investigated for its potential to enhance flap viability.

MATERIALS AND

METHODS

Firstly, this study used bioinformatics analysis to identify potential regulatory targets and signaling pathways involved in flap ischemia-reperfusion (I/R) injury. Secondly, a McFarlane random flap model (3 × 9 cm) was established on the back of rats to evaluate the effects of different doses of baicalin (60 mg/kg and 120 mg/kg, oral gavage) and JAK2-STAT3 inhibitor AG490 (1 mg/kg, intraperitoneal injection) on the random flap necrosis rate. Finally, on the 7th day after surgery, skin flap tissue was collected to evaluate the effects of baicalin on blood perfusion, neovascularization, histopathological changes, oxidative stress markers (SOD and MDA), JAK2-STAT3 signaling pathway, and apoptosis related protein (Bcl-2 and BAX) expression levels.

RESULTS

Bioinformatics analysis shows that during the stages of tissue ischemia and reperfusion, signaling pathways such as VEGF, cytokines, JAK2-STAT3, and apoptosis play important regulatory roles. In the rat random flap model, research has found that baicalin reduces the rate of flap necrosis in a dose-dependent manner. The mechanism of action includes increasing blood flow perfusion and angiogenesis, reducing I/R injury, and inhibiting the inflammatory response by inhibiting the JAK2-STAT3 signaling pathway.

CONCLUSIONS

This study confirms that baicalin can promote the survival of random flaps and reveals the mechanism.